Document Detail


Redox control of cardiac excitability.
MedLine Citation:
PMID:  22897788     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Reactive oxygen species (ROS) have been associated with various human diseases, and considerable attention has been paid to investigate their physiological effects. Various ROS are synthesized in the mitochondria and accumulate in the cytoplasm if the cellular antioxidant defense mechanism fails. The critical balance of this ROS synthesis and antioxidant defense systems is termed the redox system of the cell. Various cardiovascular diseases have also been affected by redox to different degrees. ROS have been indicated as both detrimental and protective, via different cellular pathways, for cardiac myocyte functions, electrophysiology, and pharmacology. Mostly, the ROS functions depend on the type and amount of ROS synthesized. While the literature clearly indicates ROS effects on cardiac contractility, their effects on cardiac excitability are relatively under appreciated. Cardiac excitability depends on the functions of various cardiac sarcolemal or mitochondrial ion channels carrying various depolarizing or repolarizing currents that also maintain cellular ionic homeostasis. ROS alter the functions of these ion channels to various degrees to determine excitability by affecting the cellular resting potential and the morphology of the cardiac action potential. Thus, redox balance regulates cardiac excitability, and under pathological regulation, may alter action potential propagation to cause arrhythmia. Understanding how redox affects cellular excitability may lead to potential prophylaxis or treatment for various arrhythmias. This review will focus on the studies of redox and cardiac excitation.
Authors:
Nitin T Aggarwal; Jonathan C Makielski
Related Documents :
14744808 - Sildenafil (viagra) reduces arrhythmia severity during ischaemia 24 h after oral admini...
11206718 - Norepinephrine release is increased in the hibernating heart, studied in a chronic cani...
2512008 - Electrophysiological effects of flecainide in a canine 7 day old myocardial infarction ...
7446428 - Lidocaine-induced reduction in size of experimental myocardial infarction.
2407398 - Indications for heart valve replacement.
8402768 - Intraoperative assessment of left ventricular function with transesophageal echocardiog...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2012-08-16
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  18     ISSN:  1557-7716     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2012-12-18     Completed Date:  2013-05-21     Revised Date:  2014-02-04    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  432-68     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Action Potentials
Animals
Arrhythmias, Cardiac / physiopathology
Calcium Channels, L-Type / physiology
Calcium Signaling
Heart / physiopathology*
Humans
Myocardial Contraction
Myocardium / metabolism
Oxidation-Reduction
Potassium Channels / physiology
Reactive Oxygen Species / metabolism
Sodium Channels / physiology
Grant Support
ID/Acronym/Agency:
R01HL-57414/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Calcium Channels, L-Type; 0/Potassium Channels; 0/Reactive Oxygen Species; 0/Sodium Channels
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Anion-Exchange-Driven Disassembly of a SiO(2)/CTAB Composite Mesophase: the Formation of Hollow Meso...
Next Document:  Malignant calcification is an important unfavorable prognostic factor in primary invasive breast can...